In conclusion, the phenotypic expression of apoC-I per VLDL particles is an important modulator of triglyceride metabolism in the fasting and postprandial states independent of apoC-III and traditional cardiovascular risk factors and may thereby represent an underlying mechanism for the association between the content of apoC-I per VLDL particle and carotid atherosclerosis. This evidence concerns the gene APOC1 and carotid atherosclerosis.